Respiratory pathophys Flashcards
1
Q
Upper respiratory
A
above the larynx
pharyngitis, otitis media, sinusitis
2
Q
Lower respiratory tract
A
below the larynx
acute bronchitis, chronic bronchitis, pneumonia, TB
3
Q
Defense mechanisms against infections, URT
A
nasal hairs, gag reflex, epiglottis, mucosal lymphoid tissue, secretory immunoglobulins
4
Q
Defense mechanisms against infection, LRT
A
secretory IGA, ciliated epithelium, bronchospasm, cough reflex, alveolar macrophages
5
Q
Conditions that impair host defenses
A
Cigarette smoking
Intubation
Recurrent laryngeal nerve damage
Absent gag reflex
Cystic fibrosis
Congenital absence of IgA
Oversedation
6
Q
Cigarette smoking
A
paralyzes cilia, destroys epithelium, decreases number of macrophages, decreases macrophages’ activity
7
Q
Intubation
A
impairment of host defenses, bypasses upper respiratory tract
8
Q
Recurrent laryngeal nerve damage
A
at risk during surgeries
speech, swallowing, coughing
9
Q
Absent gag reflex
A
1/3 individuals don’t have it, increased risk for aspiration
10
Q
Cystic fibrosis
A
overproduction of thick sputum, risk for increased infection
11
Q
Congenital absence of IgA
A
increased risk for infection
12
Q
Oversedation
A
decreases ability to cough
usually occurs was opiates or other CNS depressants
13
Q
Pathogenesis of lower respiratory tract infections
A
- nasopharyngeal colonization with the organism and subsequent aspiration of nasopharyngeal secretions
- reflux of GI bacteria and aspiration of contents in presence of antacid use
14
Q
Acute bronchitis
A
D: inflammation of bronchial mucosa and increased endobronchial mucus production, due to infection
E: viral and seasonal
CP: dry cough or cough with purulent or mucoid sputum. myalgias, sore throat
T: no antibiotics
15
Q
Pneumonias
A
inflammation of lungs with consolidation (something in lungs besides air
can be bacterial (community, nosocomial, aspiration), viral, mycoplasma
16
Q
Atelectasis
A
partial or complete collapse of lung
17
Q
_____ can lead to aspiration pneumonia
A
dysphagia
18
Q
Dysphagia
A
difficulty swallowing, can lead to aspiration pneumonia
19
Q
How can we prevent aspiration?
A
NPO
Positioning, semiupright in bed with HOB >30 (semi-fowler and fowler’s)
20
Q
Clinical Presentation of Bacterial pneumonia
A
abrupt onset of high fever
chills, cough with purulent sputum
chest pain, dyspnea, myalgias, malaise, tachycardia
altered mental status in elderly
21
Q
Diagnosis and Treatment of Bacterial Pneumonia
A
DX: hx, physical exam, chest xray, blood cultures, sputum culture, WBC count
Treatment: ABX, bronchodilators, airway clearance techniques
22
Q
Outcome of bacterial pneumonias
A
Good in young and middle-aged, little or no permanent defect
elderly can die, 30-50% in bacteremic pneumonia. Harder to diagnose
23
Q
Clinical presentation & Diagnosis of Viral pneumonia
A
S/S: fever, dry cough, myalgias, tachypnea, flu-like symptoms, scattered crackles, hypoxemia
DX: History, PE, CXR
24
Q
Treatment and Outcome Viral Pneumonias
A
Treatment: symptomatic, no ACTs
Outcome: usually resolvles w/out complications or lasting damage, mortality <5%.
Covid-19 is an example
25
Pleurisy
inflammation of pleural lining of the lung with exudate formation into pleural cavity (pleural effusion)
secondary to pneumonia
pleural infection w/TB or influenza
Secondary to other systemic illnesses
26
Pleurisy Clinical Presentation
Chest pain due to edema
referred to chest wall, abdomen, upper trap, shoulder
Cough, fever, tachypnea
27
Diagnosis and Treatment of Pleurisy
Dx: History & PE
pleural friction rub. splinting area of pain may decrease discomfort
Tx: time, NSAIDs, other analgesics
28
TB Etiology
acquired by inhalation of m. tuberculosis in aerosols & dusts
airborne transmission extremely efficient, droplets are sprayed by infectious individuals
thrives in crowding, poverty, poor nutrition
29
Primary Infection of TB
latent TB infection
-transient bacteremic phase brought under control by host immune system
-mild symptoms or asymptomatic
-lung lesion and enlarged lymph nodes walled off (granuloma)
30
Secondary active TB infection clinical presentation
TB disease, active TB
lapse in immune competence allows reactivation of dormant mycobacteria
any organ can be affected, lungs are the most due to high PO2
31
Dx and Tx of TB
DX = history, PE, CXR, sputum
Tx: anti-TB drug combo (isoniaxid, rifampin, ethambutol
32
Outcome and Prevention of TB
Outcome: modern cure rates are high. Development of multi-drug resistant TB (low compliance), TB is leading cause of people with HIV
Prevention: improved social conditions, immunizations, wear appropriate PPE
33
Tuberculosis Risk Factors
HIV
Diabetes
Substance abuse
Homelessness
Migrant workers
healthcare workers
jails
nursing homes
34
COPD
preventable and treatable disease
airflow limitation that is progressive
reaction to noxious particles or gases
chronic airflow limitation caused by mixture of small airway disease and parenchymal destruction
35
How does airflow obstruction occur in COPD?
Inflammation within airways
Mucus obstructs airways
Remodeling/scarring
airways collapse due to damaged parenchyma
36
How is COPD diagnosed?
S/S: shortness of breath, chronic cough, sputum
RF: host factors, tobacco, occupation, pollution
Spirometery: required to establish dx
other tests: CXR, ABGs, CBC/increased HcT
37
Clinical Features of COPD
40s to 50s with cough or acute chest illness
dyspnea on exertion
Hx of episodic wheezing and dyspnea
CXR: hyperinflated lungs, flat diaphragm, enlarged right ventricle
38
Risk factors for COPD
Environment
Host
39
Environment for COPD
Tobacco smoke
Occupational exposure
Indoor/outdoor air pollution
infections
poverty
40
Pack-year
1 pack per day x 40 years
2 packs per day x 20 years
41
Host and COPD
Genetic predisposition
specific gene abnormality (antitrupsin deficiency)
aging (increased
females
early lung development
42
____ is required to make a diagnosis of COPD
spirometry
43
FEV levels and COPD
FEV1/FVC <.70 confirms persistent airflow limitations
44
COPD Treatment Goals
Reduce Symptoms = reduce airflow obstruction, improve ex tolerance, improve QOL
Limit disease progression = prevent and treat exacerbations, reduce mortality
45
5 As of smoking cessation
Ask = identify tobacco users
Advise = 3 minute counseling session
Assess = determine willingness to quit
Assist = aid pt in quitting
Arrange = schedule f/u contact
46
5 Rs of smoking cessation
Relevance--help pt identify why quitting is relevant now
Risks--encourage them saying negative outcomes
Rewards--help pt identify benefits
Roadblocks--help identify obstacles in quitting
Repetitions--take more than 1 time to quit
47
Medications for COPD
does not stop long term decline in lung function
goals are instead to prevent/control symptoms, reduce frequency of exacerbations, improve ex tolerance
48
Drug classes for COPD
Bronchodilators
Glucocorticoids
Supplemental O2
49
Bronchodilators
prn or regular use reduce airflow obstruction
B2 adrenergic agonists, anticholinergics, methylxanthines
50
Glucocorticoids
short-term use only
prednisone
51
Supplemental O2
improve hemodynamics, lung mechanics and survival
usually for severe COPD pts with PaO2 thats less than 55
52
Treatment Options for COPD
Reduce risk factors
Drug classes for COPD
Surgery for COPD
Pulmonary Rehab
53
Surgery for COPD
Bullectomy = removal of large distended portion of lung
Lung transplantation = only in very advanced and select cases
54
Pulmonary Rehab
for improvement in dyspnea, health status, and QOL in stable pts, reducing symptoms of anxiety and depression
55
COPD Prognosis
w/out smoking cessation, lungs will continue to lose function
peripheral skeletal muscle dysfunction, muscle wasting, osteoporosis are also possible conditions.
be cautious with positioning and spinal mobs
56
Blue bloater is known as
chronic bronchitis
57
Pink puffer is known as
emphysema
58
Barrel-chested
describes the rounded, bulging chest that resembles shape of barrel
not a disease, may indicate underlying condition
59
Chronic bronchitis
chronic inflammation of bronchi/bronchioles. increased tracheobronchial mucus production sufficient to cause a cough producing sputum on most days for 3 months during consecutive years
blue bloater
60
Pathogenesis of chronic bronchitis
increased size of tracheobronchial mucus glands and increased mucus production
decreased # of cilia
bronchoconstriction due to irritation in tracheobronchial tree
61
How to improve exercise tolerance in chronic bronchitis
hydration
airway clearance techniques
ventilatory strategies
smoking cessation
prevention of infections
maintain healthy immune system
62
Emphysema
abnormal permanent enlargement of airspaces distal to terminal bronchioles accompanied by destruction of alveolar walls
can be centrilobular (more common) or panlobular
pink puffer
63
Pathogenesis of emphysema
inflammation, edema, thickened bronchiolar walls
lungs become hyperinflated, enlarged air space in parenchyma
bullae = spaces greater than 1 cm form that allow air in but not out
64
How to improve exercise tolerance for emphysema
ventilatory strategies
teach energy conservation techniques
teach breath control (pursed lip breathing)
infection control
flu shots
hydration and nutrition
65
Pores of Kohn
interalveolar connections
pausing at top of breath allows for air to disperse through alveoli
66
Cor pulmonale
right ventricular failure. causes edema (blue bloater)
67
Summary of Emphysema
60 yr old+
severe dyspnea
scanty/mucoid sputum
not frequent infections
hyperinflation, bullae
normal PaCO2, low PaO2, low hematocrit
rare for cor pulmonale
severely decreased elastic recoil
68
Summary of Chronic Bronchitis
+50 yr olds
mild dyspnea
copious, purulent sputum
frequent infections
large heart
increased PaCO2, low PaO2, increased hematocrit
common cor pulmonale
normal elastic recoil
69
Bronchiectasis
abnormal dilation and anatomical distortion of medium sized bronchi and bronchioles, associated with previous chronic necrotizing infection
w/intervention, pts can expect normal life expectancy
70
Pathogenesis of bronchiectasis
obstruction of airways and recurrent respiratory infections
mucosa destroyed, replaced by scar
damaged bronchi become permanently dilated and distorted
recurrent infections, cystic fibrosis, TB, fungal infections, kung abscesses, pneumonia
71
Clinical Presentation of Bronchiectasis
chronic productive cough
dyspnea and tachypnea
increased PCO2, decreased PO2
FINGER CLUBBING
72
Treatment Bronchiectasis
IV fluids
IV/oral ABX
hydration
Chest PT and other ACTs
education
73
Strategies to improve ex tolerance, Bronchiectasis
Hydration
ACTs
proper medication use, frequent ABX use
surgical lung resection
74
Cystic Fibrosis
genetic disorder inherited in autosomal recessive pattern. characterized by widespread abnormalities of all exocrine glands w/pathology in bronchial mucus glands, exocrine glands of pancreas, sweat glands
75
Clinical Presentation of CF
productive cough
proliferative sputum production
decreased ex tolerance
recurrent hemoptysis (bloody cough)
steatorrhea (oily stools)
76
Dx of CF
New born genetic screening test
sweat chloride test
hypoxemia, respiratory acidosis, mixed obstructive/restrictive pattern on labs
eval at CF care center
77
Treatment options for CF
ideal place to receive treatment is at a CF care center
education, bronchodilators, ACTs, exercise, pancreatic enzyme replacement, nutritional support, antibiotics, mucus thinners, modulators, lung transplantation
78
Prognosis of CF
highly variable presentation and severity
life expectancy has begun to increase
79
Strategies to improve exercise tolerance, CF
hydration
pancreatic enzymes to promote fat digestion and improve nutrition
aggressive ACTs
respiratory muscle training
strength and endurance ex
80
Asthma
chronic inflammatory disorder of airways, characterized by increased responsiveness of airway smooth muscle to various stimuli. narrowing of airways reverses either spontaneously or due to treatment
81
Epidemiology of Asthma
higher in boys, higher in women
african americans have more attacks
low income families
higher and worst incomes in rural
82
Asthma triggers
Allergic: pollen, animal dander, feathers, molds, dust, food
Nonallergic: air pollution, weather, infections, medications, emotions, exercise
83
Pathogenesis of Asthma
1.some stimulus triggers cascade inflammatory cell migration, activation.
2.process is multicellular--> mast cells, eosinophils, t-lymph, macrophages, neutrophils
3.repetitive inflammation increases bronchial hyper-reactivity
4.during acute asthma attack, lumens of airways are narrowed by combo of muscle spasm, inflammation, mucus overproduction
84
3 S's of asthma
spasm
swelling
secretions
85
Presentation of acute asthma attack
increased work of breathing and use of accessory muscles
tachypnea
audible wheezing in expiratory phase
dry cough
chest tightness
waking at night
86
Dx of asthma
no single universally accepted test
history, spirometry (improvement in FEV1 by 12-15%), peak expiratory flow rate
87
Exercise-induced asthma
transient airway obstruction occurring. also called bronchospasm. during or after exercise. usually does not involve inflammation and mucus formation
symptoms include wheezing, coughing, SOB, chest discomfort
88
Pathophysiology of EIB
1. bronchial hyper-reactivity most likely initiated by loss of airway surface liquid
2.air are humidified in conducting zone, results in cells losing water. after exercise is done, influx of water restores osmolarity
3.bronchospasm is triggered by loss of heat/water from airway
89
Diagnosis of EIB
pt self-reported symptoms
spirometry (pre and post exercise PFT)
10-15% decrease in post-exercise FEV1
90
Triggers for EIB
hyperventilation
respiratory heat loss (cold air)
increased osmolarity caused by respiratory water loss (dry air)
91
RF for EIB
80-90% of those diagnosed with asthma
winter sport athletes
92
Prevention of EIB
Good control of asthma
Pre-exercise prevention
gentle, intermittent warm-up
promote nasal breathing
vary exercise duration
incorporate proper cool down
ex in warm humid environment
93
Good control of asthma
controller medications may not prevent EIB
peak flow meter to measure amount of air flow in one fast, hard exhalation (peak expiratory flow rate)
94
Pre-exercise prevention for EIB
take 20-30 minutes before exercise to take short-acting bronchodilator. mast cell stabilizer, prevents histamine release
95
What to do during an asthma attack?
stop an activity
use rescue inhaler = short acting bronchodilator
sit up
call 911
continue to use rescue inhaler if S/S improve
96
Goals for asthma treatment
-Control for chronic respiratory S/S
-appropriate medication intervention, Controllers & Relievers
-minimize use of rescue inhalers
-patient education
-ex symptom-free
-review status frequently
97
Asthma Action Plan
everyone with asthma needs their own action plan
goal is to prevent and control asthma attacks, HCP works w/pt to create plan. Typically has a green, yellow, red level
98
Relievers
relieve acute bronchoconstriction
taken on as needed basis
may supplement controllers
relaxes smooth muscle increase airflow
types: 1. short acting beta adrenergic agonists (albuterol) 2. oral glucocorticoids (at hospital)
99
Controllers
provide long-term control by decreasing inflammation. taken daily, foundation for asthma management
types: inhaled glucocorticoids, leukotriene modifiers, long-acting Beta adrenergic agonists (salmetrol)
100
Short-acting relievers
albuterol
prednisolone
prednisone
101
Long-acting anti-inflammatory controller
salmeterol, beta 2 agonist
102
Inhaled glucocorticoid
CONTROLLER
most effective, potent, and frequently used anti-inflammatory asthma meds
fewer ADRs and shorter onset of action time than oral form
improves pulmonary function w/long term use.
103
Actions of Inhaled glucocrticoid
inhibit multiple segments of asthmatic cascade
suppress generation of cytokines
decrease population of airway eosinophils
prevent inflammatory mediator release
104
Leukotriene modifiers
oral
long-term control and prevention of symptoms
protect against EIB
decrease needed dose of inhaled glucocorticoid
anti-inflammatory
block leukotriene receptors in airways which are involved in inflammatory
105
Long acting Beta agonists
decrease frequency and intensity of asthma exacerbations
may be used as supplement to inhaled glucocorticoids
some provide prophylaxis against EIB for up to 8 hr
actions: bronchodilation--effective up to 12 hours, increase expiratory flow rate
106
Strategies we can teach to improve ex tolerance and asthma
coordinate activities w/inhalers
evaluate and instruct in proper use of MDIs
warm-up and stretch active muscles and chest wall
slow initiation and pacing, energy conservation
ventilatory strategies
incorporate cool down
hydration
107
Prognosis of asthma
variable disease course
reversible w/meds and respiratory therapy
untreated = damage
early detection is imperative
